Men's Hormone and Performance Panel

Low testosterone is a contributing factor in approximately 25 to 35% of men with erectile dysfunction (ED), though it is rarely the sole cause. More commonly, ED results from the interaction between hormonal, vascular, psychological, and neurological factors. Even when testosterone is low, addressing it with testosterone replacement therapy (TRT) improves libido and erection quality in many men — particularly those with moderate to severe deficiency. However, TRT alone may not resolve ED if vascular insufficiency (arteriogenic ED, which is the most common underlying cause in older men) or significant psychological contributors are also present.

When oestradiol is disproportionately high relative to testosterone — a pattern common in men with obesity, liver disease, or heavy alcohol use, which all increase aromatase activity — it can suppress the pituitary’s release of LH and FSH, further reducing testosterone production. Additionally, high oestradiol in men is independently associated with impaired erectile function and low libido, reduced morning erections, and gynaecomastia. The oestradiol-to-testosterone ratio is clinically as important as either value alone. Management options depend on the cause but may include weight loss (which reduces aromatase activity), treating underlying liver disease, or in some cases low-dose aromatase inhibitor therapy.

An elevated prolactin result should first be confirmed with a repeat test taken under rested conditions, since prolactin rises acutely with stress, recent sexual activity, exercise, and even the blood draw itself. If confirmed elevated (above 700 mIU/L in most male reference ranges), the most important next steps are: a medication review (antipsychotics, antiemetics, opioids, and some antidepressants all raise prolactin), thyroid testing (hypothyroidism raises prolactin), and consideration of pituitary MRI to exclude a prolactinoma. Treated prolactinoma can restore testosterone and sexual function dramatically — making this a very actionable finding.

Primary hypogonadism means the testes themselves are not producing adequate testosterone — despite strong pituitary signalling (elevated LH and FSH). Causes include Klinefelter syndrome, testicular injury or surgery, radiotherapy, mumps orchitis, and chemotherapy. Secondary hypogonadism means the problem is upstream — in the pituitary or hypothalamus — with low LH and FSH failing to adequately stimulate healthy testes. Causes include pituitary tumours, elevated prolactin, obesity (which suppresses gonadotrophin-releasing hormone (GnRH)), opioid use, and extreme stress. The distinction matters for treatment: TRT works for both, but secondary hypogonadism from reversible causes may respond to addressing the underlying issue, and fertility outcomes differ significantly.

TRT improves sexual desire (libido) very reliably in men with confirmed hypogonadism, and often improves erection quality — particularly morning erections and erection firmness. However, it does not reliably resolve arteriogenic ED (where blood flow to the penis is physically impaired by vascular disease) or psychogenic ED (where anxiety, relationship issues, or performance anxiety are the primary drivers). Many men find that TRT plus a phosphodiesterase-5 inhibitor (such as sildenafil or tadalafil) together address both the hormonal and vascular components more effectively than either alone. Your physician report will recommend appropriate next steps based on your full result pattern.